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I&I WC2 > Clinical pharmacology III > Flashcards

Clinical pharmacology III Flashcards

1
Q

What are the two main causes of chronic kidney disease?

A
  1. Diabetes
  2. Hypertension
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2
Q

How can glomerular kidney disease present itself? (2)

A
  1. Nephrotic
  2. Nephritic
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3
Q

What are the characteristics of nephrotic syndrome? (4)

A
  1. Fatty urine casts
  2. Proteinuria > 3.5 g/day
  3. Hematuria +/-
  4. Kidney disease, without primarily inflammation
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4
Q

What are the clinical features of nephrotic syndrome? (3)

A
  1. Generalized edema
  2. Periorbital edema
  3. HTN
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5
Q

What are the characteristics of nephritic syndrome? (3)

A
  1. RBC casts
  2. Proteinuria < 3.5 g/day
  3. Inflammation of the glomerulus
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6
Q

What are the clinical features of nephritic syndrome? (2)

A
  1. HTN
  2. Edema
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7
Q

What are examples of primary glomerular kidney diseases? (5)

A
  1. Minimal change disease
  2. Primary focal- and segmental glomerulosclerosis
  3. Membranous nephropathy
  4. Membranoproliferative glomerulonephritis
  5. IgA nephropathy
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8
Q

What are examples of secondary glomerular kidney diseases? (6)

A
  1. Lupus nephritis
  2. Anti-GBM disease
  3. Amyloidosis
  4. Infection-related GN
  5. ANCA-associated vasculitis
  6. Atypical HUS
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9
Q

Which factors can you measure in a blood test to determine if someone has glomerular kidney disease? (5)

A
  1. Anti-nuclear antibodies (ANA)
  2. Anti-neutrophil cytoplasmic antibodies (ANCA)
  3. Anti-GBM antibodies
  4. Complement C3 and C4
  5. Underlying disease: M protein, virology
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10
Q

What is the most common cause of nephrotic syndrome? Due to what?

A

Membranous nephropathy -> due to anti-PLA2R antibodies

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11
Q

What are the histopathological features of membranous nephropathy?

A

Subepithelial deposits (Spikes) on top of GBM and podocytes are fused

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12
Q

Membranous nephropathy: what are the subepithelial deposits (spikes) visual on EM most likely?

A

Antibody/immune complexes

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13
Q

What is the role of M-type phospholipase A2 receptor in membranous nephopathy?

A

Target antigen

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14
Q

Where is M-type phospholipase A2 receptor present?

A

Podocytes

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15
Q

True or false: patients have antibodies against the M-type phospholipase A2 receptor

A

True

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16
Q

What are the steps in the pathogenesis of membranous nephropathy? (4)

A
  1. Immune complex formation in kidney
  2. Complement activation
  3. Damage of podocytes
  4. Proteinuria
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17
Q

Which two processes can lead to autoimmunity in membranous nephropathy?

A
  1. Processing of PLA2R antigen into soluble form
  2. Endocytosis of PLA2R antigen
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18
Q

How does processing of PLA2R antigen into soluble form lead to autoimmunity in membranous nephropathy? (6)

A
  1. Antigen binding to autoreactive B cell
  2. Antigen fragmentation
  3. Antigen uptake and presentation to T cell
  4. Cytokine released from stimulated T cells
  5. Affinity maturation/CSR
  6. Increased frequency of autoreactive B cells occurring over time
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19
Q

How does endocytosis of PLA2R antigen lead to autoimmunity of membranous nephropathy?

A
  1. APCs take up antigen
  2. Co-
  3. Affinity maturation/CSR
  4. Increased frequency of autoreactive B cells occurring over time
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20
Q

What is the prognosis of glomerular disease?

A

75-100% survival after 15 years depending on the disease

21
Q

Which patients are at a higher risk of a bad prognosis for glomerular kidney disease? (3)

A
  1. > 3.5gr/day
  2. Decrease of kidney function at baseline
  3. Male
22
Q

Why do you definitely start treatment of higher risk glomerular kidney patients?

A

To prevent progression to end-stage kidney disease

23
Q

What are treatment options for kidney disease to prevent kidney failure? (2)

A
  1. Dialysis
  2. Kidney transplantation
24
Q

Which cells can you target to combat the autoimmune part of membranous nephropathy? (3)

A
  1. Targeting T cells and cytokines
  2. Targeting APCs and T cells
  3. Targeting B cells, plasma cells and complement
25
Q

True or false: kidney disease patients treated with rituximab have a better outcome than kidney disease patients treated with cyclosporine

26
Q

Kidney disease patients: If rituximab doesn’t work, what kind of treatment do you give these patients? (2)

A
  1. Cyclophosphamide (chemo)
  2. Prednison
27
Q

What can be a side-effect of treating kidney disease patients with rituximab or cyclosporine?

A

Kaposi sarcoma

28
Q

What is a hallmark of hemolytic uremic syndrome (HUS)?

A

Thrombotic microangiopathy

29
Q

What are the characteristics of thrombotic microangiopathy? (3)

A
  1. Hemolysis
  2. Lack of thrombocytes
  3. Decrease kidney function
30
Q

What are the three main characteristics of HUS?

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. Acute kidney injury
31
Q

What does microangiopathic hemolytic anemia entail? (2)

A
  1. Small vessel disease
  2. Destruction of red blood cells
32
Q

How does the destruction of red blood cells in microangiopathic hemolytic anemia look when studying a biopsy?

A
  1. Narrowing of red arterioles
  2. Endothelium of capillaries are swollen (activation of endothelium)
33
Q

What are the four underlying diseases leading to HUS?

A
  1. Infection-induced HUS
  2. HUS with coexisting diseases or conditions
  3. Cobalamin C defect- HUS
  4. Atypical HUS
34
Q

What are the four types of infection-induced HUS?

A
  1. S.pneumoniae-HUS
  2. STEC-HUS
  3. Influenza A, H1N1
  4. HIV
35
Q

When does infection-induced HUS occur?

A

Comes in outbreaks (poisoned food)

36
Q

What are examples of HUS with coexisting diseases or conditions? (6)

A
  1. HSCT/solid organ transplantation
  2. AID
  3. Malignancy
  4. Drugs
  5. Malignant hypertension
  6. Pre-existing nephropathy
37
Q

What causes atypical HUS?

A

Complement regulation disorder

38
Q

What are the three types of atypical HUS?

A
  1. DGKE-HUS
  2. HUS with dysregulation of the complement alternative pathway
  3. HUS without identified complement or DGKE mutation or anti-CFH antibody
39
Q

What underlying mechanisms cause HUS with dysregulation of the complement alternative pathway?

A
  1. Mutations in CGH, CFI, MCP, C3, CFB, THBD
  2. Anti-CFH antibody
40
Q

Complement: all three pathways lead to? (3)

A
  1. Inflammation
  2. Membrane attack complex
  3. Opsonization
41
Q

Eventueel complement pathway specifics

42
Q

What do the membrane attack complex and/or C5a activate/induce in atypical HUS?

A
  1. WIth C5a: activation of platelets
  2. RBC lysis
  3. Endothelial cell damage
  4. C5a: induces clot formation
43
Q

HUS: What can go wrong in regulation? (2)

A
  1. Gene mutations (C regulating genes)
    2 Anti-factor H antibodies
44
Q

Which gene mutations can occur in HUS? (4)

A
  1. Factor H,I (soluble)
  2. CD46/MCP (membrane bound)
  3. C3, GOF (factor H binding, soluble)
  4. Factor B (soluble)
45
Q

HUS: How do you treat patients if there is something wrong in the regulation of complement?

A
  1. Plasma exchange
  2. Kidney transplantation
  3. Eculizumab/ravulizumab
46
Q

HUS: When is there a risk of recurrence after kidney transplantation?

A

If a soluble factor is still present after Tx

47
Q

Where does eculizumab (anti-CD5) interfere in the alternative pathway?

A

Prevents C5 cleavage and MAC formation

48
Q

What is the downside of eculizumab?

I&I WC2 (16 decks)

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